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The 12 cranial nerves

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This is the date the draft was written, not a medical review date.

A comparison table of the twelve cranial nerves, followed by links to a short article on each.

Scan the table to compare the nerves side by side, then open a nerve for its own article. The Roman numerals I to XII follow the order of the table.

The twelve cranial nerves
No.NerveTypeNucleiExit from the skullFunctionBedside testingLesion signs
I (1)Olfactory nerveSensoryThe first-order neurons are the bipolar receptor cells of the olfactory epithelium. Their axons end on mitral and tufted cells in the olfactory bulb, whose axons form the olfactory tract and project to the anterior olfactory nucleus and primary olfactory cortex.The fila olfactoria pass through the foramina of the cribriform plate of the ethmoid bone to reach the olfactory bulb lying on its upper surface in the anterior cranial fossa.Special visceral afferent (smell) only. Olfactory information reaches the primary olfactory cortex (piriform cortex, amygdala) without a compulsory thalamic relay, which is unusual among sensory systems.Test each nostril separately with the other occluded, using a mild non-irritant familiar odour (for example coffee or soap) with the eyes closed. Avoid pungent substances such as ammonia, which stimulate the trigeminal nerve instead.Unilateral or bilateral loss of smell (anosmia) or reduced smell (hyposmia) ipsilateral to the lesion. Taste is often reported as impaired because flavour depends largely on smell. Foster Kennedy syndrome combines ipsilateral anosmia and optic atrophy with contralateral papilloedema from a frontal mass.
II (2)Optic nerveSensoryOrigin: retinal ganglion cells. Main termination: lateral geniculate nucleus of the thalamus (relay to the primary visual cortex via the optic radiations). Other targets: pretectal nuclei (pupillary reflex), superior colliculus (visual reflexes) and suprachiasmatic nucleus (circadian rhythm).The nerve leaves the orbit through the optic canal of the lesser wing of the sphenoid, accompanied by the ophthalmic artery and the meningeal sheaths, and joins its fellow at the optic chiasm above the pituitary gland.Special somatic afferent (vision). Retinal ganglion cell axons convey light information; the nasal retinal fibres cross at the optic chiasm, so each optic tract carries the contralateral visual hemifield. Afferent limb of the pupillary light reflex.Test visual acuity (Snellen chart, with correction), colour vision (Ishihara plates), visual fields by confrontation, the direct and consensual pupillary light reflexes, the swinging-light test for a relative afferent pupillary defect, and fundoscopy of the optic disc.Optic nerve lesion: monocular visual loss with a relative afferent pupillary defect and reduced colour vision. Chiasmal lesion: bitemporal hemianopia. Optic tract or radiation lesion: contralateral homonymous hemianopia; temporal lobe (Meyer loop) lesions give a superior quadrantanopia, parietal lesions an inferior one.
III (3)Oculomotor nerveMotorOculomotor nucleus (somatic) at the level of the superior colliculus in the midbrain, and the Edinger-Westphal nucleus (parasympathetic) lying dorsally and rostrally to it. The levator palpebrae is supplied by a single midline caudal subnucleus, so ptosis from a nuclear lesion is bilateral.It passes through the cavernous sinus and enters the orbit through the superior orbital fissure, where it divides into a superior division (superior rectus, levator palpebrae) and an inferior division (medial and inferior rectus, inferior oblique, parasympathetic root to the ciliary ganglion).General somatic efferent to the superior, inferior and medial rectus, inferior oblique and levator palpebrae superioris. General visceral efferent (parasympathetic) to the sphincter pupillae and ciliary muscle via the ciliary ganglion.Test eye movements in the H pattern, looking for diplopia, ptosis, and failure of adduction, elevation or depression. Examine pupil size and the direct and consensual light reflexes, and the accommodation reflex (near response).Complete palsy gives ptosis, and the eye is deviated down and out (unopposed lateral rectus and superior oblique) with a dilated, poorly reactive pupil. Pupil-sparing palsy suggests ischaemia of the nerve trunk (for example diabetes); a dilated pupil suggests external compression.
IV (4)Trochlear nerveMotorTrochlear nucleus in the caudal midbrain at the level of the inferior colliculus, ventral to the cerebral aqueduct. Fibres pass dorsally, decussate in the superior medullary velum and emerge contralaterally, so the muscle is supplied by the opposite nucleus.It runs around the cerebral peduncle, through the cavernous sinus, and enters the orbit through the superior orbital fissure above the common tendinous ring to reach the superior oblique.General somatic efferent to the superior oblique, which depresses and intorts the eye, most effectively when the eye is adducted. It is important for looking down and inward, for example when reading or walking downstairs.Ask the patient to look down and in (adducted and depressed gaze) while observing for diplopia and failure of depression. Vertical diplopia worse on looking down, for example on stairs, and a head tilt are typical complaints.Vertical or oblique diplopia, maximal on downward gaze with the eye adducted. The affected eye is slightly elevated, and patients typically tilt the head away from the side of the lesion to minimise the diplopia. A nuclear lesion affects the contralateral eye.
V (5)Trigeminal nerveMixedThree sensory nuclei: the main (principal) sensory nucleus in the pons for touch and discriminative sensation, the spinal trigeminal nucleus extending to the upper cervical cord for pain and temperature, and the mesencephalic nucleus for proprioception from the masticatory muscles. The motor nucleus lies in the pons.V1 leaves through the superior orbital fissure, V2 through the foramen rotundum and V3 through the foramen ovale. The sensory root arises from the trigeminal ganglion in Meckel's cave; the small motor root joins V3 below the ganglion.General somatic afferent (touch, pain, temperature, proprioception) from the face, scalp anterior to the vertex, cornea, nasal and oral mucosa, teeth, and most of the dura. Special visceral efferent to the muscles of mastication, tensor tympani, tensor veli palatini, mylohyoid and anterior belly of digastric.Test light touch and pinprick in all three divisions bilaterally, the corneal reflex (afferent V1, efferent VII), and the jaw jerk. Test the motor part by palpating the masseters and temporalis during clenching and by asking the patient to open the mouth against resistance (the jaw deviates toward the weak side).Sensory loss in one or more divisions on the face with an absent corneal reflex on the affected side. Motor lesion produces ipsilateral weakness of mastication, with the jaw deviating toward the lesion on opening. A lesion of the spinal trigeminal nucleus or tract gives ipsilateral facial loss of pain and temperature.
VI (6)Abducens nerveMotorAbducens nucleus in the pons, in the floor of the fourth ventricle, encircled by the fibres of the facial nerve (the facial colliculus). It lies close to the paramedian pontine reticular formation (horizontal gaze centre).It emerges at the pontomedullary junction, ascends the clivus, bends over the petrous apex beneath the petroclinoid ligament (Dorello canal), runs through the cavernous sinus next to the internal carotid artery, and enters the orbit via the superior orbital fissure.General somatic efferent to the lateral rectus only, producing abduction of the eye. The nucleus also contains interneurons that project via the medial longitudinal fasciculus to the contralateral oculomotor nucleus for conjugate horizontal gaze.Ask the patient to follow a target laterally in each direction, observing for failure of abduction, the position of the eyes at rest, and diplopia that is horizontal and maximal on looking toward the affected side.The affected eye is medially deviated (convergent squint) at rest because of unopposed medial rectus action, with horizontal diplopia worst on looking toward the side of the lesion (lateral gaze). A pontine nuclear lesion causes an ipsilateral gaze palsy rather than an isolated abduction deficit.
VII (7)Facial nerveMixedFacial motor nucleus in the caudal pons (its upper part, supplying the forehead, receives bilateral corticonuclear input); superior salivatory and lacrimal nuclei (parasympathetic); and the nucleus of the solitary tract (rostral gustatory part) for taste.It enters the internal acoustic meatus with CN VIII, runs in the facial canal of the temporal bone (giving the greater petrosal nerve, nerve to stapedius and chorda tympani), and exits the skull through the stylomastoid foramen, then divides within the parotid gland into temporal, zygomatic, buccal, marginal mandibular and cervical branches.Special visceral efferent to the muscles of facial expression, stapedius, stylohyoid and posterior belly of digastric. Special visceral afferent (taste) from the anterior two thirds of the tongue via the chorda tympani. General visceral efferent (parasympathetic) to lacrimal, nasal, submandibular and sublingual glands. Small general somatic afferent component from the external ear.Ask the patient to raise the eyebrows, close the eyes tightly against resistance, show the teeth, smile and puff the cheeks. Compare the forehead (frontalis) with the lower face. Taste of the anterior tongue, lacrimation (Schirmer test) and hyperacusis (stapedius) can be assessed when localisation is needed.Lower motor neuron (nuclear or nerve) lesion paralyses the whole ipsilateral face, including the forehead. An upper motor neuron lesion spares the forehead because of bilateral cortical innervation of the upper face, producing contralateral weakness of the lower face only. Higher lesions in the facial canal add loss of taste, reduced lacrimation or hyperacusis.
VIII (8)Vestibulocochlear nerveSensoryDorsal and ventral cochlear nuclei at the pontomedullary junction (then superior olivary complex, lateral lemniscus, inferior colliculus and medial geniculate nucleus to the auditory cortex, Brodmann areas 41 and 42). Four vestibular nuclei (superior, inferior, medial, lateral) in the floor of the fourth ventricle, with connections to the cerebellum, spinal cord and ocular motor nuclei.Both parts travel with the facial nerve through the internal acoustic meatus of the petrous temporal bone, cross the cerebellopontine angle cistern and enter the brainstem at the pontomedullary junction, lateral to the facial nerve.Special somatic afferent. The cochlear division conveys sound from the hair cells of the organ of Corti (spiral ganglion). The vestibular division conveys head acceleration and position from the semicircular canals, utricle and saccule (vestibular ganglion of Scarpa).Hearing: whisper or finger-rub test, then Rinne and Weber tuning-fork tests to distinguish conductive from sensorineural loss, with audiometry for confirmation. Vestibular: assess nystagmus, the head impulse test, gait and Romberg test, and the Dix-Hallpike manoeuvre for positional vertigo.Cochlear lesion: sensorineural hearing loss and tinnitus. Vestibular lesion: vertigo, nystagmus (fast phase away from a peripheral lesion), nausea and imbalance. Because central auditory pathways are bilateral, unilateral central lesions rarely cause marked deafness.
IX (9)Glossopharyngeal nerveMixedNucleus ambiguus (motor to stylopharyngeus), inferior salivatory nucleus (parasympathetic), nucleus of the solitary tract (taste and visceral afferents including the carotid sinus), and the spinal trigeminal nucleus (general sensation).It leaves the skull through the jugular foramen, together with CN X and CN XI, passes between the internal carotid artery and the internal jugular vein, and curves forward around stylopharyngeus to reach the pharynx and tongue.General somatic and visceral afferent from the pharynx, tonsil, posterior third of the tongue, middle ear and carotid sinus (baroreceptors) and body (chemoreceptors). Special visceral afferent (taste, posterior third). Special visceral efferent to stylopharyngeus. General visceral efferent to the parotid gland via the otic ganglion.Test the gag reflex (afferent IX, efferent X) and the palatal movements, and assess the taste and general sensation of the posterior third of the tongue when needed. Isolated IX lesions are uncommon and are usually assessed together with the vagus nerve.Loss of the gag reflex on the affected side (afferent limb), loss of taste and sensation over the posterior third of the tongue, and mild dysphagia. Glossopharyngeal lesions usually coexist with vagal and accessory involvement in jugular foramen syndromes.
X (10)Vagus nerveMixedNucleus ambiguus (motor to pharynx and larynx, and cardiac parasympathetic neurons), dorsal motor nucleus of the vagus (parasympathetic to thoracic and abdominal viscera), nucleus of the solitary tract (visceral afferents and taste), and the spinal trigeminal nucleus (somatic sensation).It leaves the skull through the jugular foramen, descends in the carotid sheath, and passes through the thorax and the oesophageal hiatus of the diaphragm into the abdomen. The right recurrent laryngeal nerve loops around the right subclavian artery, the left around the aortic arch, then both ascend in the tracheo-oesophageal groove.Special visceral efferent to the muscles of the palate (except tensor veli palatini), pharynx and larynx. General visceral efferent (parasympathetic) to the heart, lungs and gut. General and special visceral afferent from the viscera and the epiglottic taste buds, and general somatic afferent from the external ear and meninges.Ask the patient to say 'ah' and watch the soft palate rise symmetrically with the uvula in the midline, assess voice quality (hoarseness) and cough, and test swallowing. Laryngoscopy is needed to assess vocal cord movement.A unilateral lesion causes the soft palate to droop on the affected side and the uvula to deviate away from the lesion toward the normal side on phonation, with hoarseness, dysphagia and a weak cough. Recurrent laryngeal nerve injury causes hoarseness from vocal cord paralysis; bilateral injury may cause stridor and airway compromise.
XI (11)Accessory nerveMotorSpinal accessory nucleus in the lateral part of the anterior horn of the upper cervical cord (roughly C1 to C5 or C6). The cranial fibres originate from the nucleus ambiguus. Supranuclear control for the sternocleidomastoid is ipsilateral in effect (turns the head to the opposite side), and for the trapezius is mainly contralateral.The spinal roots ascend alongside the cord, enter the skull through the foramen magnum, and leave through the jugular foramen. The nerve then passes to the sternocleidomastoid and crosses the posterior triangle of the neck superficially to reach the trapezius.Special visceral efferent (classically described) to sternocleidomastoid and trapezius. The cranial root, which joins the vagus nerve to supply laryngeal muscles, is now generally regarded as part of the vagus. Proprioceptive fibres arrive from the cervical plexus.Ask the patient to shrug the shoulders against resistance (trapezius) and to turn the head against the examiner's hand (sternocleidomastoid; the muscle on the side opposite to the direction of turning is tested). Inspect for wasting, shoulder drooping and winging.Ipsilateral weakness of the trapezius (drooping shoulder, weak shrug, difficulty abducting the arm above horizontal) and of the sternocleidomastoid (weak head rotation toward the opposite side). A jugular foramen lesion usually also involves CN IX and X.
XII (12)Hypoglossal nerveMotorHypoglossal nucleus in the medulla, in the floor of the fourth ventricle near the midline (hypoglossal trigone). Corticonuclear input is predominantly crossed for genioglossus, so a supranuclear lesion causes tongue deviation away from the side of the cortical lesion.Rootlets emerge between the pyramid and the olive in the medulla, unite and leave the skull through the hypoglossal canal of the occipital bone. The nerve then descends between the internal carotid artery and the internal jugular vein, loops forward above the hyoid bone and enters the tongue.General somatic efferent to the muscles of the tongue (genioglossus, hyoglossus, styloglossus and the intrinsic muscles). Genioglossus protrudes the tongue, so its action on protrusion is the basis of the bedside test.Inspect the tongue at rest for wasting and fasciculations, then ask the patient to protrude the tongue and observe for deviation, and to push the tongue against each cheek against resistance. Assess speech and swallowing.In a lower motor neuron lesion the tongue deviates toward the side of the lesion on protrusion (the unopposed healthy genioglossus pushes it toward the weak side), with ipsilateral wasting and fasciculations. In a supranuclear lesion there is no wasting and the tongue deviates away from the cortical lesion, toward the weak side of the body.

References

  1. Drake RL, Vogl AW, Mitchell AWM. Gray's Anatomy for Students. Elsevier — Tier 3 (textbook)
  2. Moore KL, Dalley AF, Agur AMR. Clinically Oriented Anatomy. Wolters Kluwer, 8th edition (2018) — Tier 3 (textbook)
  3. Haines DE, Mihailoff GA. Fundamental Neuroscience for Basic and Clinical Applications. Elsevier, 5th edition (2018) — Tier 3 (textbook)
  4. Kandel ER, Koester JD, Mack SH, Siegelbaum SA. Principles of Neural Science. McGraw-Hill, 6th edition (2021) — Tier 3 (textbook)
  5. Bickley LS. Bates' Guide to Physical Examination and History Taking (Bickley). Wolters Kluwer, 13th edition (2020) — Tier 3 (textbook)

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